Two distinct mechanisms for experience-dependent homeostasis

Michelle C.D. Bridi, Roberto De Pasquale, Crystal L. Lantz, Yu Gu, Andrew Borrell, Se Young Choi, Kaiwen He, Trinh Tran, Su Z. Hong, Andrew Dykman, Hey Kyoung Lee, Elizabeth M. Quinlan, Alfredo Kirkwood

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Models of firing rate homeostasis such as synaptic scaling and the sliding synaptic plasticity modification threshold predict that decreasing neuronal activity (for example, by sensory deprivation) will enhance synaptic function. Manipulations of cortical activity during two forms of visual deprivation, dark exposure (DE) and binocular lid suture, revealed that, contrary to expectations, spontaneous firing in conjunction with loss of visual input is necessary to lower the threshold for Hebbian plasticity and increase miniature excitatory postsynaptic current (mEPSC) amplitude. Blocking activation of GluN2B receptors, which are upregulated by DE, also prevented the increase in mEPSC amplitude, suggesting that DE potentiates mEPSCs primarily through a Hebbian mechanism, not through synaptic scaling. Nevertheless, NMDA-receptor-independent changes in mEPSC amplitude consistent with synaptic scaling could be induced by extreme reductions of activity. Therefore, two distinct mechanisms operate within different ranges of neuronal activity to homeostatically regulate synaptic strength.

Original languageEnglish (US)
Pages (from-to)843-850
Number of pages8
JournalNature neuroscience
Issue number6
StatePublished - Jun 1 2018

ASJC Scopus subject areas

  • General Neuroscience


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